Roles of mTORC1 and mTORC2 in controlling γδ T1 and γδ T17 differentiation and function.

ABSTRACT: The metabolism-controlled differentiation of αβ T cells has been well documented; however, the role of a metabolism program in γδ T cell differentiation and function has not been clarified. Here, using CD2-cre; mTORC1 Raptor-f/f, and mTORC2 Rictor-f/f mice (KO mice), we found that mTORC1, but not mTORC2, was required for the proliferation and survival of peripheral γδ T cells, especially Vγ4 γδ T cells. Moreover, mTORC1 was essential for both γδ T1 and γδ Τ17 differentiation, whereas mTORC2 was required for γδ T17, but not for γδ Τ1, differentiation. We further studied the underlying molecular mechanisms and found that depletion of mTORC1 resulted in the increased expression of SOCS1, which in turn suppressed the key transcription factor Eomes, consequentially reducing IFN-γ production. Wh

SUBMITTER: Yang Q 

PROVIDER: S-EPMC7308385 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature